Evidence map›Paper›PMID 35840921›Full record

ArticleBMC cancer2022

ASIC1α up-regulates MMP-2/9 expression to enhance mobility and proliferation of liver cancer cells via the PI3K/AKT/mTOR pathway.

Yinci Zhang, Jiaojiao Liang, Niandie Cao, Jiafeng Gao, Yinghai Xie, Shuping Zhou, Xiaolong Tang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 30 citations in OpenAlex.

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  5. Cannabidiol-Ion Channel Interactions Represent a Promising Preventive and Therapeutic Strategy in Hepatocellular Carcinoma.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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  13. CTLA-4 silencing could promote anti-tumor effects in hepatocellular.Medical oncology (Northwood, London, England) · 2024
    Article
  14. Article
  15. Article
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Yinci Zhang *Medcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Jiaojiao Liang *Medcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Niandie Cao *Medcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Jiafeng Gao *Medcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Yinghai XieMedcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Shuping ZhouMedcial School, Anhui University of Science & Technology, Huainan, 232001, China.
Xiaolong TangMedcial School, Anhui University of Science & Technology, Huainan, 232001, China. txljd2006@126.com.
Anhui University of Science and Technology · CNWuhu Institute of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major challenge in the treatment of liver cancer is that a large proportion of patients fail to achieve long-term disease control, with death from liver cancer cell migration and invasion. Acid-sensitive ion channel 1α (ASIC1α) is involved in the migration, invasion, and proliferation of liver cancer cells. Therefore, we explored the mechanism of ASIC1α-mediated liver cancer cell migration and invasion. We determined the levels of ASIC1α by western blotting and immunofluorescence in HepG2 and SK-Hep1 cells cultured in various acidic conditions. In addition, wound healing assay, transwell invasion assay, and MTT assay were conducted to assess the migration, invasion, and proliferation abilities of liver cancer cells. Western blotting was conducted to determine the levels of MMP2, MMP9, ASIC1α, p-PI3Kp85, t-PI3Kp85, p-AKT(Ser473), t-AKT, p-mTOR (Ser2448), t-mTOR. We first found that the levels of ASIC1α in the HepG2 and SK-Hep1 cells in acidic conditions (pH 6.5) were significantly increased. Inhibition and knockdown of ASIC1α down-regulated MMP-2/9 expression and inhibited the migration, invasion, and proliferation of HepG2 and SK-Hep1 cells; overexpression of ASIC1α had the opposite effect. We further demonstrated that ASIC1α up-regulates MMP-2/9 via activation of the PI3K/AKT/mTOR pathway, thereby promoting migration, invasion, and proliferation of liver cancer cells. Overexpression of MMP-2/9 and activation of AKT reversed these effects on liver cancer cells caused by inhibition of ASIC1α. We conclude that ASIC1α can regulate migration, invasion, and proliferation of liver cancer cells through the MMP-2/9/PI3K/AKT/mTOR pathway. These observations may provide a new reference for liver cancer chemotherapy.

Indexed as

Acid Sensing Ion ChannelsLiver NeoplasmsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCell Line, TumorCell MovementCell ProliferationHumansNeoplasm InvasivenessSignal TransductionAcid Sensing Ion ChannelsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAcid-sensitive ion channel 1αHepG2 cellsLiver cancerMMP-2/9PI3K/AKT/mTORSK-Hep1cells

Identifiers

PMID35840921
PMCPMC9287982
OpenAlexW4285588322

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.